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case
Itchy Lesions on the Back of the Leg
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BACKGROUNDA 32-year-old man presents to the emergency
department with an itchy and painful rash on the back of his left
leg (see Image). About 7 days ago, he began to feel an “intense,
burning” pain behind his left knee. Over the subsequent days, “small
blisters” began to “pop up” over the area but were the worst behind
the knee itself. He treated the lesion with an over-the-counter
antibiotic ointment and acetaminophen (Tylenol), but they did not
relieve the pain. Any contact, however slight, with the apparent blisters
immediately intensifies the pain. The patient reports having fevers, sneezing,
and a runny nose over the last 2 weeks. He
does not report any cough, shortness of breath, headaches,
or fatigue. He also reports extreme stress at work with
many deadlines and an ongoing threat of job loss because of
continuing downsizing due to overseas corporate operations. He denies exposing the
affected area to heat or cold (burn) or to
chemical agents, including detergents or cleaning agents. He has
not started taking any new medications recently and is currently taking
only acetaminophen. He has no known drug allergies, he quit
smoking tobacco several years ago, and he drinks
alcohol only rarely. His medical history is significant only for an
appendectomy. On physical examination, the patient’s vital signs are a temperature
of 37.2°C, a heart rate of 82 beats per
minute, and a blood pressure of 124/67 mm
Hg. Lesions are observed on the back of
the left knee (see Image), and similar but smaller lesions
appear in a bandlike distribution along the posterior length of
his left leg up to the buttock region. The
affected leg is neurovascularly intact. Remaining findings on
neurologic examination, cardiorespiratory examination, and the review of systems are
unremarkable.
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***** HINT *****
Consider the intense, burning pain occurring in a bandlike distribution.
***** ANSWER *****
Herpes zoster (shingles): Herpes zoster is a viral
infection caused by the varicella-zoster virus (VZV), the same virus that
leads to chickenpox on initial exposure, which is usually in childhood.
After the initial exposure and chickenpox resolves, the virus remains
latent in the posterior spinal or cranial sensory ganglia for the person’s
lifetime. Focal reactivation along the ganglial distribution in adulthood
leads to herpes zoster. Factors responsible for reactivating the virus are
not well delineated but may include depression of the immune system,
trauma, advanced age, exposure to radiation, certain medications,
infection, or stress. Most cases are relatively mild and occur along an
isolated dermatomal distribution (see Image 2). Paresthesias or pain along
the affected dermatome usually precede the disease. However, severe or
complicated cases can also occur. For example, especially in
immunocompromised patients, multidermatomal reactivation and dissemination
can occur with hematogenous spread, bacterial superinfection leading to
sepsis, or CNS and visceral involvement. Other specific complications such as meningoencephalitis, transverse myelitis,
cranial-nerve palsies, granulomatous angiitis, hepatitis, and pneumonitis can also occur. Granulomatous
angiitis may result in a cerebrovascular accident. In addition, reactivation along
the ophthalmic division of the trigeminal nerve can lead to ocular involvement
and herpes zoster ophthalmicus with a resultant risk for conjunctivitis,
keratitis, corneal ulceration, iridocyclitis, glaucoma, and blindness. Involvement of the
nasociliary branch often appears as a single lesion on the tip of
the nose (ie, Hutchinson sign). Failure to perform slit-lamp examination with fluorescein
stain to identify the dendritic corneal lesions may lead to a missed
diagnosis of herpetic zoster ophthalmicus. Involvement of the geniculate ganglion can produce Ramsay
Hunt syndrome or herpes zoster oticus. This involvement is characterized
by pain in the external ear, external auditory
canal, and tympanic membrane. Transient, unilateral facial paralysis is not uncommon.
Ramsay Hunt syndrome can be associated with vertigo, tinnitus, and hearing disorders.
In uncomplicated cases affecting a single dermatome, the
chief morbidity is intense, burning pain. The vesicles may become superinfected but usually resolve in
14-21 days. After the vesicular rash resolves, patients may
develop postherpetic neuralgia, a common complication characterized by pain that
persists for longer than 1 month.
This complication is most common in patients older than
50 years, and its intensity can be incapacitating. The diagnosis is primarily based
on the patient’s clinical history and physical findings.
Laboratory tests (eg, Tzanck smear, direct immunofluorescence
assay, polymerase chain reaction [PCR]) or viral cultures
may be useful in difficult cases. The classic histologic findings
are multinucleated giant cells with an accentuation of nuclear material at the
periphery of the nuclei. The mainstays of treatment are
antiviral therapy and analgesia. For patients with a distribution in
a single dermatome, initial therapy may include nonsteroidal anti-inflammatory drugs (NSAIDs)
with narcotics for analgesia. Dressings wetted with tap water or
5% aluminum acetate (Burow solution) may be applied to the affected skin
for 30-60 minutes 4-6 times per day. Lotions (eg, calamine
lotion) may also help relieve the discomfort. Oral antiviral
therapy decreases pain, shortens the duration of the lesions,
reduces the incidence of complications, and lowers the incidence
of postherpetic neuralgia if it is started within 48 hours of the onset of the lesions.
Some practitioners extend this window to 72 hours. Patients with disseminated zoster, multidermatomal involvement, suspected
or known CNS involvement or relative immunosuppression should be treated with
parenteral acyclovir and admitted to the hospital. Finally, large-controlled trials have investigated
the role of steroids in combination with antiviral therapy, demonstrating improvement in the healing
rate of lesions and time to resolution of acute pain. Caution should be exercised
when prescribing steroids to patients with certain medical conditions (eg, diabetes mellitus, gastritis) that may be
exacerbated by the side effects of this class of drugs.
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Authors:
Martin I. Newman, MD, Associate Staff, Department of
Plastic and Reconstructive Surgery, Cleveland Clinic
Florida, Weston Margaret J. Gorensek, MD, FACP, FAAP, Department
of Plastic and Reconstructive Surgery and the Department of Infectious Diseases,
Cleveland Clinic Florida Rick Kulkarni,
MD, Attending Physician, Director of Informatics, Department of Emergency
Medicine, Olive View - UCLA Medical Center, Assistant Professor
of Medicine, David Geffen School of Medicine
at UCLA
References:
Chang AK. Osgood-Schlatter Disease. eMedicine journal
[serial online]. February 10, 2005. Available at:
www.emedicine.com/emerg/topic347.htm. Accessed November 14, 2005. Ozonoff MB.
Pediatric Orthopedic Radiology. 2nd ed. Philadelphia, PA: WB Saunders 1992:
371-2. Resnick D. Diagnosis of Bone and Joint Disorders. 4th ed. Philadelphia,
PA: WB Saunders; 2002: 3729-30, 3714-8. Wheeless’ Textbook of Orthopedics.2005.
Data Trace Publishing Company. Available at: www.wheelessonline.com. Accessed
November 14, 2005
eMedicine Editor:
Luis
Lovato, MD, Attending Physician, Director of Critical
Care, Department of Emergency Medicine, Olive View - UCLA Medical Center,
Assistant Professor of Medicine, David Geffen School of Medicine at UCLA
Source
http://emedicine.com
Jan 2006
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